Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

2.respiratory infections


Published on

Published in: Education, Health & Medicine
  • Be the first to comment

2.respiratory infections

  1. 1. Respiratory Infections
  2. 2. Respiratory tract defences <ul><li>Ventilatory flow </li></ul><ul><li>Cough </li></ul><ul><li>Mucociliary clearance mechanisms </li></ul><ul><li>Mucosal immune system </li></ul>
  3. 3. Upper respiratory tract infections <ul><li>Rhinitis </li></ul><ul><ul><li>Rhinovirus, coronavirus, influenza/parainfluenza </li></ul></ul><ul><ul><li>Non-infective (allergic) rhinitis has similar symptoms (related to asthma) </li></ul></ul><ul><li>Sinusitis </li></ul><ul><li>Otitis media </li></ul><ul><li>Latter 2 have a risk of bacterial superinfection, mastoiditis, meningitis, brain abscess </li></ul>
  4. 4. Laryngitis <ul><li>Most commonly upper respiratory viruses </li></ul><ul><li>Diphtheria </li></ul><ul><ul><li>C. diphtheriae produces a cytotoxic exotoxin causing tissue necrosis at site of infection with associated acute inflammation. Membrane may narrow airway and/or slough off (asphyxiation) </li></ul></ul>
  5. 6. Acute epiglottitis <ul><li>H. influenza type B </li></ul><ul><li>Another cause of acute severe airway compromise in childhood </li></ul>
  6. 7. Pneumonia <ul><li>Infection of pulmonary parenchyma with consolidation </li></ul>
  7. 8. Pneumonia <ul><li>Gr. “disease of the lungs” </li></ul><ul><li>Infection involving the distal airspaces usually with inflammatory exudation (“localised oedema”). </li></ul><ul><li>Fluid filled spaces lead to consolidation </li></ul>
  8. 9. Classification of Pneumonia <ul><li>By clinical setting (e.g. community acquired pneumonia) </li></ul><ul><li>By organism (mycoplasma, pneumococcal etc) </li></ul><ul><li>By morphology (lobar pneumonia, bronchopneumonia) </li></ul>
  9. 10. Pathological description of pneumonia
  10. 11. Organisms <ul><li>Viruses – influenza, parainfluenza, measles, varicella-zoster, respiratory syncytial virus (RSV). Common, often self limiting but can be complicated </li></ul><ul><li>Bacteria </li></ul><ul><li>Chlamydia, mycoplasma </li></ul><ul><li>Fungi </li></ul>
  11. 12. Lobar Pneumonia <ul><li>Confluent consolidation involving a complete lung lobe </li></ul><ul><li>Most often due to Streptococcus pneumoniae (pneumococcus) </li></ul><ul><li>Can be seen with other organisms (Klebsiella, Legionella) </li></ul>
  12. 13. Clinical Setting <ul><li>Usually community acquired </li></ul><ul><li>Classically in otherwise healthy young adults </li></ul>
  13. 14. Pathology <ul><li>A classical acute inflammatory response </li></ul><ul><ul><li>Exudation of fibrin-rich fluid </li></ul></ul><ul><ul><li>Neutrophil infiltration </li></ul></ul><ul><ul><li>Macrophage infiltration </li></ul></ul><ul><ul><li>Resolution </li></ul></ul><ul><li>Immune system plays a part antibodies lead to opsonisation, phagocytosis of bacteria </li></ul>
  14. 15. Macroscopic pathology <ul><li>Heavy lung </li></ul><ul><ul><li>Congestion </li></ul></ul><ul><ul><li>Red hepatisation </li></ul></ul><ul><ul><li>Grey hepatisation </li></ul></ul><ul><ul><li>Resolution </li></ul></ul><ul><ul><li>The classical pathway </li></ul></ul>
  15. 16. Lobar pneumonia (upper lobe – grey hepatisation), terminal meningitis
  16. 17. Pneumonia – fibrinopurulent exudate in alveoli (grossly “red hepatisation”)
  17. 18. Pneumonia – neutrophil and macrophage exudate (grossly “grey hepatisation”)
  18. 19. Complications <ul><li>Organisation (fibrous scarring) </li></ul><ul><li>Abscess </li></ul><ul><li>Bronchiectasis </li></ul><ul><li>Empyema (pus in the pleural cavity) </li></ul>
  19. 20. Pneumonia – fibrous organisation
  20. 21. Bronchopneumonia <ul><li>Infection starting in airways and spreading to adjacent alveolar lung </li></ul><ul><li>Most often seen in the context of pre-existing disease </li></ul>
  21. 22. Bronchopneumonia
  22. 23. Bronchopneumonia <ul><li>The consolidation is patchy and not confined by lobar architecture </li></ul>
  23. 24. Clinical Context <ul><li>Complication of viral infection (influenza) </li></ul><ul><li>Aspiration of gastric contents </li></ul><ul><li>Cardiac failure </li></ul><ul><li>COPD </li></ul>
  24. 25. Organisms <ul><li>More varied – Strep. Pneumoniae, Haemophilus influenza, Staphylococcus, anaerobes, coliforms </li></ul><ul><li>Clinical context may help. Staph /anaerobes/coliforms seen in aspiration </li></ul>
  25. 26. Complications <ul><li>Organisation </li></ul><ul><li>Abscess </li></ul><ul><li>Bronchiectasis </li></ul><ul><li>Empyema </li></ul>
  26. 27. Viral pneumonia <ul><li>Gives a pattern of acute injury similar to adult respiratory distress syndrome (ARDS) </li></ul><ul><li>Acute inflammatory infiltration less obvious </li></ul><ul><li>Viral inclusions sometimes seen in epithelial cells </li></ul>
  27. 28. The immunocompromised host <ul><li>Virulent infection with common organism (e.g. TB) – the African pattern </li></ul><ul><li>Infection with opportunistic pathogen </li></ul><ul><ul><li>virus (cytomegalovirus - CMV) </li></ul></ul><ul><ul><li>bacteria ( Mycobacterium avium intracellulare) </li></ul></ul><ul><ul><li>fungi (aspergillus, candida, pneumocystis) </li></ul></ul><ul><ul><li>protozoa (cryptosporidia, toxoplasma) </li></ul></ul>
  28. 29. Diagnosis <ul><li>High index of suspicion </li></ul><ul><li>Teamwork (physician, microbiologist, pathologist) </li></ul><ul><li>Broncho-alveolar lavage </li></ul><ul><li>Biopsy (with lots of special stains!) </li></ul>
  29. 30. Immunosuppressed patient – fatal haemorrhage into Aspergillus-containing cavity
  30. 31. HIV-positive patient CMV (cytomegalovirus) and “pulmonary oedema” on transbronchial biopsy….
  31. 32. Special stain also shows Pneumocystis
  32. 33. Tuberculosis <ul><li>22 million active cases in the world </li></ul><ul><li>1.7 million deaths each year (most common fatal organism) </li></ul><ul><li>Incidence has increased with HIV pandemic </li></ul>
  33. 34. Tuberculosis <ul><li>Mycobacterial infection </li></ul><ul><li>Chronic infection described in many body sites – lung, gut, kidneys, lymph nodes, skin…. </li></ul><ul><li>Pathology characterised by delayed (type IV) hypersensitivity (granulomas with necrosis) </li></ul>
  34. 35. Tuberculosis (pathogenesis of clinical disease) <ul><li>Virulence of organisms </li></ul><ul><li>Hypersensitivity vs. immunity </li></ul><ul><li>Tissue destruction and necrosis </li></ul>
  35. 36. Mycobacterial virulence <ul><li>Related to ability to resist phagocytosis. </li></ul><ul><li>Surface LAM antigen stimulates host tumour necrosis factor (TNF)  production (fever, constitutional symptoms) </li></ul>
  36. 37. Organisms <ul><li>M. tuberculosis/M.bovis main pathogens in man </li></ul><ul><li>Others cause atypical infection especially in immunocompromised host. Pathogenicity due to ability; </li></ul><ul><ul><li>to avoid phagocytosis </li></ul></ul><ul><ul><li>to stimulate a host T-cell response </li></ul></ul>
  37. 38. Immunity and Hypersensitivity <ul><li>T-cell response to organism enhances macrophage ability to kill mycobacteria </li></ul><ul><ul><li>this ability constitutes immunity </li></ul></ul><ul><li>T-cell response causes granulomatous inflammation, tissue necrosis and scarring </li></ul><ul><ul><li>this is hypersensitivity (type IV) </li></ul></ul><ul><li>Commonly both processes occur together </li></ul>
  38. 39. Pathology of Tuberculosis (1) <ul><li>Primary TB (1st exposure) </li></ul><ul><ul><li>inhaled organism phagocytosed and carried to hilar lymph nodes. Immune activation (few weeks) leads to a granulomatous response in nodes (and also in lung) usually with killing of organism. </li></ul></ul><ul><ul><li>in a few cases infection is overwhelming and spreads </li></ul></ul>
  39. 40. Pathology of Tuberculosis (2) <ul><li>Secondary TB </li></ul><ul><ul><li>reinfection or reactivation of disease in a person with some immunity </li></ul></ul><ul><ul><li>disease tends initially to remain localised, often in apices of lung. </li></ul></ul><ul><ul><li>can progress to spread by airways and/or bloodstream </li></ul></ul>
  40. 41. Tissue changes in TB <ul><li>Primary </li></ul><ul><ul><li>Small focus (Ghon focus) in periphery of mid zone of lung </li></ul></ul><ul><ul><li>Large hilar nodes (granulomatous) </li></ul></ul><ul><li>Secondary </li></ul><ul><ul><li>Fibrosing and cavitating apical lesion (cancer an important differential diagnosis </li></ul></ul>
  41. 42. Primary and secondary TB <ul><li>In primary the site of infection shows non-specific inflammation with developing granulomas in nodes </li></ul><ul><li>In secondary there are primed T cells which stimulate a localised granulomatous response </li></ul>
  42. 43. Primary TB – Ghon Focus
  43. 44. Secondary TB <ul><li>Necrosis </li></ul><ul><li>Fibrosis </li></ul><ul><li>Cavitation </li></ul><ul><li>T cell response: CD4 (helper) enhance killing. CD8 (cytotoxic) kill infected cells giving necrosis </li></ul>
  44. 45. Granulomatous inflammation with caseous necrosis
  45. 46. Acid fast stain – spot the organism (a red snapper)!
  46. 47. Complications <ul><li>Local spread (pleura, lung) </li></ul><ul><li>Blood spread. Miliary TB or “end-organ” disease (kidney, adrenal etc.) </li></ul><ul><li>Swallowed - intestines </li></ul>
  47. 48. The host-organism balance <ul><li>Not all infected get clinical disease </li></ul><ul><li>Organisms frequently persist following resolution of clinical disease </li></ul><ul><li>Any diminished host resistance can reactivate (thus 33% of HIV positive are co-infected with TB </li></ul>
  48. 49. Secondary TB – rapid death due to miliary disease
  49. 50. Miliary white foci – blood spread to lower lobe
  50. 51. “ Galloping consumption” – TB bronchopneumonia
  51. 52. Decreased immunity – many more organisms on acid fast stain
  52. 53. Why does disease reactivate? <ul><li>Decreased T-cell function </li></ul><ul><ul><li>age </li></ul></ul><ul><ul><li>coincident disease (HIV) </li></ul></ul><ul><ul><li>immunosuppressive therapy (steroids, cancer chemotherapy) </li></ul></ul><ul><li>Reinfection at high dose or with more virulent organism </li></ul>
  53. 54. Lung Abscess <ul><li>Localised collection of pus. Central tissue destruction. Lined by granulation tissue/fibrosis (attempted healing) </li></ul><ul><li>Tumour-like </li></ul><ul><li>Chronic malaise and fever </li></ul>
  54. 55. Lung abscess <ul><li>Organisms: </li></ul><ul><ul><li>Staphylococcus </li></ul></ul><ul><ul><li>Anaerobes </li></ul></ul><ul><ul><li>Gram negatives </li></ul></ul><ul><li>Clinical contexts: </li></ul><ul><ul><li>Aspiration </li></ul></ul><ul><ul><li>Following pneumonia </li></ul></ul><ul><ul><li>Fungal infection </li></ul></ul><ul><ul><li>Bronchiectasis </li></ul></ul><ul><ul><li>Embolic </li></ul></ul>
  55. 56. Bronchiectasis <ul><li>Abnormal fixed dilatation of the bronchi </li></ul><ul><li>Usually due to fibrous scarring following infection (pneumonia, tuberculosis, cystic fibrosis) </li></ul><ul><li>Also seen with chronic obstruction (tumour) </li></ul><ul><li>Dilated airways accumulate purulent secretions </li></ul>
  56. 57. Bronchiectasis (2) <ul><li>Affects lower lobes preferentially </li></ul><ul><li>Chronic recurring infection sometimes leads to finger clubbing </li></ul>
  57. 58. Complications of bronchiectasis <ul><li>Pneumonia </li></ul><ul><li>Abscess </li></ul><ul><li>Septicaemia </li></ul><ul><li>Empyema </li></ul><ul><li>“ Metastatic” abscess </li></ul><ul><li>Amyloidosis </li></ul>
  58. 59. Bronchiectasis with chronic suppuration
  59. 60. Bronchiectasis
  60. 61. Bronchiectasis distal to an obstructing tumour